Sleep deprivation linked to skin aging

Main Category: Dermatology
Also Included In: Sleep / Sleep Disorders / Insomnia;  Seniors / Aging
Article Date: 26 Jul 2013 - 0:00 PDT Current ratings for:
Sleep deprivation linked to skin aging

In a first-of-its-kind clinical trial, physician-scientists at University Hospitals (UH) Case Medical Center found that sleep quality impacts skin function and aging. The recently completed study, commissioned by Estee Lauder, demonstrated that poor sleepers had increased signs of skin aging and slower recovery from a variety of environmental stressors, such as disruption of the skin barrier or ultraviolet (UV) radiation. Poor sleepers also had worse assessment of their own skin and facial appearance.

The research team, led by Primary Investigator Elma Baron, MD, presented their data this spring at the International Investigative Dermatology Meeting in Edinburgh, Scotland in an abstract titled "Effects of Sleep Quality on Skin Aging and Function."

"Our study is the first to conclusively demonstrate that inadequate sleep is correlated with reduced skin health and accelerates skin aging. Sleep deprived women show signs of premature skin aging and a decrease in their skin's ability to recover after sun exposure," said Dr. Baron, Director of the Skin Study Center at UH Case Medical Center and Associate Professor of Dermatology at Case Western Reserve University School of Medicine. "Insufficient sleep has become a worldwide epidemic. While chronic sleep deprivation has been linked to medical problems such as obesity, diabetes, cancer and immune deficiency, its effects on skin function have previously been unknown."

Skin functions as an important barrier from external stressors such as environmental toxins and sun-induced DNA damage. The research team set out to determine if skin function and appearance is also impacted by sleep quality, which is vital to the growth and renewal of the body's immune and physiological systems.

The study involved 60 pre-menopausal women between the ages of 30 and 49, with half of participants falling into the poor quality sleep category. The classification was made on the basis of average duration of sleep and the Pittsburgh Sleep Quality Index, a standard questionnaire-based assessment of sleep quality. The study involved a visual skin evaluation and participation in several non-invasive skin challenge tests including UV light exposure and skin barrier disruption. Additionally, participants filled out a sleep log for one week to quantify sleep duration.

The researchers found statistically significant differences between good and poor quality sleepers. Using the SCINEXA skin aging scoring system, poor quality sleepers showed increased signs of intrinsic skin aging including fine lines, uneven pigmentation and slackening of skin and reduced elasticity. In this system, a higher score means a more aged appearance. The average score in the good quality sleepers was 2.2 versus 4.4 in poor quality sleepers. They found no significant difference between the groups in signs of extrinsic aging, which are attributed primarily to sun exposure, such as coarse wrinkles and sunburn freckles.

The researchers found that good quality sleepers recovered more efficiently from stressors to the skin. Recovery from sunburn was more sluggish in poor quality sleepers, with erythema (redness) remaining higher over 72 hours, indicating that inflammation is less efficiently resolved. A Transepidermal Water Loss (TEWL) test was used at various time points to determine the ability of the skin to serve as an effective barrier against moisture loss. In measurements 72 hours after a skin barrier stressor (tape-stripping), the recovery of good quality sleepers was 30% higher than poor quality sleepers (14% vs. -6%) demonstrating that they repair the damage more quickly.

Additionally, poor quality sleepers were significantly more likely to have a higher Body Mass Index (BMI). For example, 23% of good quality sleepers were obese compared to 44% of poor quality sleepers. Not surprisingly, self perception of attractiveness was significantly better in good quality sleepers (mean score of 21 on self evaluation) vs. poor quality sleepers (mean score of 18).

"This research shows for the first time, that poor sleep quality can accelerate signs of skin aging and weaken the skin's ability to repair itself at night," said Dr. Daniel Yarosh, Senior Vice President, Basic Science Research, R&D, at The Estée Lauder Companies. "These connections between sleep and skin aging, now supported with solid scientific data, will have a profound effect on how we study skin and its functions. We see these findings as yet another way we can direct our scientific research toward the real needs of our customers who want to look and feel their best."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Study Links Vitamin D Deficiency To Accelerated Aging Of Bones

Main Category: Bones / Orthopedics
Also Included In: Nutrition / Diet;  Seniors / Aging
Article Date: 14 Jul 2013 - 0:00 PDT Current ratings for:
Study Links Vitamin D Deficiency To Accelerated Aging Of Bones

Everyone knows that as we grow older our bones become more fragile. Now a team of U.S. and German scientists led by researchers with the U.S. Department of Energy (DOE)'s Lawrence Berkeley National Laboratory (Berkeley Lab) and the University of California (UC) Berkeley has shown that this bone-aging process can be significantly accelerated through deficiency of vitamin D - the sunshine vitamin.

Vitamin D deficiency is a widespread medical condition that has been linked to the health and fracture risk of human bone on the basis of low calcium intake and reduced bone density. However, working at Berkeley Lab's Advanced Light ALS), a DOE national user facility, the international team demonstrated that vitamin D deficiency also reduces bone quality.

"The assumption has been that the main problem with vitamin D deficiency is reduced mineralization for the creation of new bone mass, but we've shown that low levels of vitamin D also induces premature aging of existing bone," says Robert Ritchie, who led the U.S. portion of this collaboration. Ritchie holds joint appointments with Berkeley Lab's Materials Sciences Division and the University of California (UC) Berkeley's Materials Science and Engineering Department.

"Unraveling the complexity of human bone structure may provide some insight into more effective ways to prevent or treat fractures in patients with vitamin D deficiency," says Björn Busse, of the Department of Osteology and Biomechanics at the University Medical Center in Hamburg, Germany, who led the German portion of the team.

Ritchie and Busse have reported their findings in the journal Science Translational Medicine. The paper is titled "Vitamin D Deficiency Induces Early Signs of Aging in Human Bone, Increasing the Risk of Fracture." Co-authors also include Hrishikesh Bale, Elizabeth Zimmermann, Brian Panganiban, Holly Barth, Alessandra Carriero, Eik Vettorazzi, Josef Zustin, Michael Hahn, Joel Ager, Klaus Püschel and Michael Amling.

Vitamin-D is essential for the body to absorb calcium. The body normally synthesizes vitamin D in the skin following exposure to sunlight - hence the "sunshine" moniker. However, when vitamin D serum concentrations become deficient, the body will remove calcium from bone to maintain normal calcium blood levels. This removal of calcium from existing bone hampers the mineralization process required for the formation of new bone mass. In children, vitamin D deficiency can lead to rickets. In adults, vitamin D deficiency causes osteomalacia, a softening of the bones associated with defective mineralization that results in bone pain, muscle weakness, and increased risk of bone deformation and fracture. While treatments with vitamin D and calcium supplements are effective, success has been achieved with only modest increases in bone mineral density, suggesting other factors also play a role in reducing fracture risks.

"We hypothesized that restoring the normal level of vitamin D not only corrects the imbalance of mineralized and non-mineralized bone quantities, but also initiates simultaneous multiscale alterations in bone structure that affects both the intrinsic and extrinsic fracture mechanisms," Ritchie says.

To test this hypothesis, Busse and his German team collected samples of iliac crest bone cores from 30 participants, half of whom were deficient in vitamin D and showed early signs of osteomalacia. For this study, a normal vitamin D level was defined as a serum concentration of 20 micrograms per liter or higher. For the vitamin D deficiency group the mean serum concentration was 10 micrograms per liter.

The bone samples were sent to Ritchie and his team for analysis at the ALS using Fourier Transform Infrared (FTIR) spectroscopy and X-ray computed microtomography. The FTIR spectroscopy capabilities of ALS beamlines 1.4.3 and 5.4.1 provide molecular-level chemical information, and ALS Beamline 8.3.2 provides non-destructive 3D imaging at a resolution of approximately one micron.

"We were interested in spatially resolved data that would help us to follow the formation of cracks under mechanical loading," Ritchie says. "The ALS beamlines enabled us to measure the structure/composition and mechanical properties of the bone samples at different size-scales, ranging from nanometers to micrometers. We measured the resistance to crack growth and by following crack growth in real-time were able to observe how cracks and structure interact. This enabled us to relate mechanical properties to specific structural changes."

Ritchie and his team found that while vitamin D-deficient subjects had less overall mineralization due to a reduction of mineralized bone, underneath the new non-mineralized surfaces, the existing bone was actually more heavily mineralized, and displayed the structural characteristics - mature collagen molecules and mineral crystals - of older and more brittle bone.

"These islands of mineralized bone were surrounded by a collagenous boundary that prevented them from being properly remodeled," Busse says. "Cut off from a supply of osteoclasts, the cells that normally remodel the bone, these isolated sections of mineralized bone begin to age, even as overall bone mineralization decreases from a lack of calcium."

Says Ritchie, "In situ fracture mechanics measurements and CT-scanning of the crack path indicated that vitamin D deficiency increases both the initiation and propagation of cracks by 22- to 31-percent."

From their study, Busse, Ritchie and their co-authors say that vitamin-D levels should be checked and kept on well-balanced levels to maintain the structural integrity of bones and avoid mineralization defects and aging issues that can lead to a risk of fractures.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our bones / orthopedics section for the latest news on this subject.

The Berkeley portion of this work was supported by Berkeley Lab’s Laboratory Directed Research and Development program. The German portion was supported by the Federal Ministry of Education and Research. Berkeley Lab’s Advanced Light Source is supported by DOE’s Office of Science.

DOE/Lawrence Berkeley National Laboratory

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